Abstract

Background

We examined differences in pathogenicity in pigs from China that had been experimentally
infected with porcine reproductive and respiratory syndrome virus (PRRSV).

Methods

We compared pathogenic characteristics of a field isolate (GX-1/2008F), two PRRSV
isolates (HN-1/2008, YN-1/2008) propagated in cells, and GX-1/2008F that had been
propagated in cells (GX-1/2008). The clinical courses, along with humoral and cell-mediated
responses, were monitored for 21 days post-infection (DPI). Animals were sacrificed
and tissue samples used for gross pathological, histopathological and ultrastructure
examination.

Results

At 2–3 DPI, animals infected with cell-propagated viruses exhibited signs of coughing,
anorexia and fever. However their rectal temperature did not exceed 40.5°C. Viremia
was detectable as early as 3 DPI in animals infected with HN-1/2008 and YN-1/2008.
Animals inoculated with GX-1/2008F displayed clinical signs at 6 DPI; the rectal temperature
of two animals in this group exceeded 41.0°C, with viremia first detected at 7 DPI.
Seroconversion for all challenged pigs, except those infected with GX-1/2008, was
seen as early as 7 DPI. All of these pigs had fully seroconverted by 11 DPI. All animals
challenged with GX-1/2008 remained seronegative until the end of the experiment. Innate
immunity was inhibited, with levels of IFN-α and IL-1 not significantly different
between control and infected animals. The cytokines IFN-γ and IL-6 transiently increased
during acute infection. All virus strains caused gross lesions including multifocal
interstitial pneumonia and hyperplasia of lymph nodes. Inflammation of the stomach
and small intestine was also observed. Lesions in the group infected with GX-1/2008F
were more serious than in other groups. Transmission electron microscopy revealed
that alveolar macrophages, plasmacytes and lymphocytes had fractured cytomembranes,
and hepatocytes had disrupted organelles and swollen mitochondria.

Conclusions

The pathogenicity of the PRRSV field isolate became attenuated when propagated in
MARC-145 cells. Tissue tropism of highly pathogenic strains prevailing in China was
altered compared with classical PRRSV strains. The observed damage to immune cells
and modulation of cytokine production could be mechanisms that PRRSV employs to evade
host immune responses.